Age-associated cognitive decline, memory in particular, is a typical consequence of aging and an increasing biomedical concern, as over 38 million individuals are age 65 and older, and by 2030 this number is projected to rise to 71 million.Recent studies support an emerging hypothesis that aberrant changes of specific histone acetylation marks in chromatin of the aging brain drives cognitive decline and specifically, memory impairment; however the specific histone acetyltransferases (HATs) involved in this process remain to be identified.As synaptic function is central for learning and memory, we use the Drosophila neuromuscular junction (NMJ) as a well-characterized synapse model to identify HATs that control synaptic plasticity and structure.